Renal dysfunction in cardiovascular diseases and its consequences

Giacomo Deferrari, Adriano Cipriani, Edoardo La Porta, Giacomo Deferrari, Adriano Cipriani, Edoardo La Porta

Abstract

It is well known that the heart and kidney and their synergy is essential for hemodynamic homeostasis. Since the early XIX century it has been recognized that cardiovascular and renal diseases frequently coexist. In the nephrological field, while it is well accepted that renal diseases favor the occurrence of cardiovascular diseases, it is not always realized that cardiovascular diseases induce or aggravate renal dysfunctions, in this way further deteriorating cardiac function and creating a vicious circle. In the same clinical field, the role of venous congestion in the pathogenesis of renal dysfunction is at times overlooked. This review carefully quantifies the prevalence of chronic and acute kidney abnormalities in cardiovascular diseases, mainly heart failure, regardless of ejection fraction, and the consequences of renal abnormalities on both organs, making cardiovascular diseases a major risk factor for kidney diseases. In addition, with regard to pathophysiological aspects, we attempt to substantiate the major role of fluid overload and venous congestion, including renal venous hypertension, in the pathogenesis of acute and chronic renal dysfunction occurring in heart failure. Furthermore, we describe therapeutic principles to counteract the major pathophysiological abnormalities in heart failure complicated by renal dysfunction. Finally, we underline that the mild transient worsening of renal function after decongestive therapy is not usually associated with adverse prognosis. Accordingly, the coexistence of cardiovascular and renal diseases inevitably means mediating between preserving renal function and improving cardiac activity to reach a better outcome.

Keywords: Acute kidney injury; Cardiovascular disease; Chronic kidney disease; Heart failure; Venous congestion; Worsening renal function.

Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Incidence of CKD or GFR decline > 5 ml/min/year in patients with chronic heart failure (CHF) (156,743) or without CHF (3,414,122) (f up 3.6 year) (Drawn from data by George LK et al. Circ Heart Fail 2017 [54])
Fig. 2
Fig. 2
One-year death or urgent heart transplantation in acute heart failure (AHF) (594 patients) on the basis of worsening renal function (WRF) and signs of congestion at discharge (Adapted from Metra M et al. Circ Heart Fail 2012 [73])
Fig. 3
Fig. 3
Pathophysiology of cardiorenal syndrome in subclinical cardiovascular disorders (CVD) or coronary, cerebrovascular and peripheral artery diseases without heart failure (HF)
Fig. 4
Fig. 4
Pathophysiology of cardiorenal syndrome in heart failure (HF)
Fig. 5
Fig. 5
Impact of acute reduction in cardiac output (CO) and/or in systolic blood pressure (SBP)/effective arterial volume on renal function in heart failure (HF) (forward mechanism). AVP arginine vasopressin, CVP central venous pressure, GFR glomerular filtration rate, RAAS renin–angiotensin–aldosterone system, RBF renal blood flow, SNS sympathetic nervous system
Fig. 6
Fig. 6
Impact of congestion on kidney function in heart failure (HF) (backward mechanism). CVP central venous pressure, GFR glomerular filtration rate, RAAS renin–angiotensin–aldosterone system, RBF renal blood flow, SNS sympathetic nervous system
Fig. 7
Fig. 7
Mortality according to hemoconcentration and worsening renal function (WRF) in 1019 patients with acute heart failure (AHF) (Adapted from Breidthardt T et al. Eur J Heart Fail 2017 [75])

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